Lack of association between TREM-1 gene polymorphisms and severe sepsis in a Chinese Han population

Summary Triggering receptor expressed on myeloid cells–1 (TREM-1) is a cell surface receptor expressed on neutrophils and monocytes. TREM-1 acts to amplify inflammation and serves as a critical mediator of inflammatory response in the context of sepsis. Blocking of TREM-1 can protect against sepsis...

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Veröffentlicht in:Human immunology 2008-03, Vol.69 (3), p.220-226
Hauptverfasser: Chen, QiXing, Zhou, HuiDan, Wu, ShuiJing, Wang, HaiHong, Lv, Chen, Cheng, BaoLi, Xie, GuoHao, Fang, XiangMing
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Sprache:eng
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Zusammenfassung:Summary Triggering receptor expressed on myeloid cells–1 (TREM-1) is a cell surface receptor expressed on neutrophils and monocytes. TREM-1 acts to amplify inflammation and serves as a critical mediator of inflammatory response in the context of sepsis. Blocking of TREM-1 can protect against sepsis in mice. To date, the predisposition of TREM-1 gene polymorphisms to sepsis has not been reported. This study was designed to investigate whether TREM-1 genomic variations were associated with the development of severe sepsis. Three common polymorphisms (rs7768162, rs9471535, and rs2234237) within the TREM-1 gene were detected in 175 patients with severe sepsis and in 139 healthy control subjects. Neither allelic frequencies nor genotype distributions of the assayed single nucleotide polymorphisms were found to be significantly different between patients and controls as well as between surviving and nonsurviving patients in different models of inheritance. The distributions of estimated haplotype patterns were also comparable between the defined groups. The present findings suggest that the three studied polymorphisms within the TREM-1 gene may not play a major role in the predisposition to severe sepsis in a Chinese Han cohort. Further replication studies with large sample size to achieve sufficient power (80%) to dismiss these polymorphisms as candidate markers for severe sepsis are warranted.
ISSN:0198-8859
1879-1166
DOI:10.1016/j.humimm.2008.01.013